Bacterial translocation, infection and coagulation in cirrhosis and portal hypertension

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In cirrhotic patients there is an increased susceptibility to bacterial infection, related to the degree of liver dysfunction leading to several abnormalities of defense mechanisms, all of which increase the susceptibility to infection, including deficiency of bactericidal and opsonic activities, impaired monocyte function, depressed phagocytic activity of the reticuloendothelial system (RES), defective chemotaxis, and low levels of complement in serum. A particularly important role is played by the reduced RES activity, which is due to the presence of extrahepatic shunts and intrahepatic shunts through sinusoids without Kupffer cells, a reduced number of Kupffer cells, and impaired Kupffer cell function. Thus cirrhotics with impaired RES phagocytic activity (as assessed by the elimination of 99m technetium-sulfur colloid) develop acute bacterial infections more frequently than cirrhotics with normal RES phagocytic activity. Both community and hospital acquired bacterial infections are frequently diagnosed in cirrhotics, the most frequent being spontaneous bacterial peritonitis (SBP), urinary tract infections, pneumonia and skin infections, their incidence increasing with the severity of liver dysfunction. Importantly, half of these episodes may be asymptomatic. Recently bacterial infections and/or endotoxaemia have been associated with failure to control variceal bleeding, more early variceal rebleeding, abnormalities in coagulation, vasodilatation of the systemic vasculature and worsening of liver function. There is an increased recognition that bacterial infections are involved in several pathophysiological abnormalities in cirrhosis, so that in this introduction we aim to evaluate the potential mechanisms and the clinical evidence illustrating the pivotal role of bacterial infection. This could lead to new treatment strategies.